The origin of bubonic plague

Although some forms of the bacterium Yersinia are harmless, other forms
have devastated human populations, causing a plague of biblical proportions (Psalm 91:3–7, 9, 10). Bubonic plague, also known as the ‘Black
Death’ that killed one fourth of Europe’s population in the 1300s, appeared
as a great pestilence several times in the Old Testament, including in Psalm 91 and in 2 Sam 24:14–25. Perhaps the clearest
example of such a plague is recorded in 1 Sam. 6:4–19, where there is a specific reference
to the tumors on people (bubos = the tumors of lymph glands) and to rats (the animal
vector that carried the plague bacterium, Yersinia pestis.) The biblical
time frame for the plagues described in 1 Samuel was about 3,000 years ago.1 Interestingly, experts on
plague ‘evolution’ estimate the emergence of Y. pestis at about
1,500–20,000 years ago (within an evolutionary timeframe, of course).2

Plague’s origin is multifaceted

The story of Yersinia’s degeneration into the plague pathogen may serve
as a model of ‘fast’ genomic decay and corruption.

Many infectious diseases can be traced back to the decay and corruption of the original
created design of microorganisms as a result of the Fall. Corruption literally means
to destroy (from the Latin corruptus). The origin of pathogenic (disease-causing)
bacteria such as Y. pestis is complex and multifaceted, and may be explained
by a combination of genes that were lost, added and moved. The story of Yersinia’s
degeneration into the plague pathogen may serve as a model of ‘fast’
genomic decay and corruption.2

It appears that the beginning of pathogenicity in the genus Yersina started
with a net loss of chromosomal DNA from its original ‘kind’ (figure
1). Later, there were minor additions of plasmid DNA3 as well as DNA from viruses and other bacteria.
A few plasmid genes for toxins (table 1) have been acquired from another existing
species, but many chromosomal genes have been lost. It takes only a few such genetic
changes to produce a new, extremely infectious variant,4 so it may have taken only hundreds or a few thousand
years to produce the current bubonic plague strain that has existed for about the
last 500 years.

Loss of chromosomal DNA

Figure 1. Origin of plague: the decay and corruption of nonpathogenic
Yersinia to highly virulent Y. pestis in a few thousand years.
Click
here for larger view

Researchers hypothesize that key chromosomal genes (i.e. involved in
metabolic pathways) were inactivated/lost in changing from a soil-inhabiting Yersinia
to a pathogenic Yersinia species.2 Pathogenic Yersiniae
have lost structural information and function in about 149 genes. Of these, 58 are
the result of frameshift mutations,5
32 have undergone deletions, and the rest are nonsense mutations.6 These incomplete/inactivated genes or ‘pseudogenes’
are an important feature of the Y. pestis genome.7

Wren2 suggests that the genes lost in Y. pestis affected bioenergetic
functions, including dicarboxylic amino-acid metabolism. This reduction of metabolic
pathways may have allowed the bacterium to conserve energy. The newly emerged strains
(variants) were thus streamlined, which might have contributed to the development
of pathogenicity (i.e. plague) due to the genes they lacked. The absence of important
biosynthetic genes is believed to be a hallmark of genome decay.

Genes added and moved

The corruption by three genes of a relatively benign recent ancestor of Y. pestis
may have played a key role in the emergence of bubonic plague. Hinnebusch and colleagues,
a plague expert team at the National Institutes for Health,8 maintains that the acquisition of two plasmid genes
(i.e. just a few discrete genetic changes) in recent times changed the fairly harmless,
Y. pseudotuberculosis, that causes mild food poisoning, to the agent of
the ‘Black Death’. A third gene (carried on plasmid pMT1) produces murine
toxin, an enzyme required for the initial survival of Y. pestis bacilli
in the flea midgut (table 1).7 By acquiring this last gene from another
organism, Y. pestis made a crucial shift in its host range, allowing it
to survive in fleas, and devolved to relying on its blood-feeding host for transmission.
This is just another example of the flexibility of many microbes in sometimes repackaging
themselves into more dangerous agents of infectious disease.

This last corruption is one that distinguishes Yersinia pestis from all
closely related, more benign bacteria such as Y. pseudotuberculosis and
other Yersinia (e.g. Y. entercolitica).7 In turn, as
Y. pestis adapted to rely on its new blood-feeding host for transmission,
the emergence of more deadly bacterial strains would have been favoured. It appears
that these minor plasmid additions10
were the last changes made in an otherwise long series of genetic losses in Y. pseudotuberculosis’
chromosome (figure 1).

One pathogenicity island was acquired by Yersinia pestis from a different
bacterium.2 This cassette of genes was not the result of evolution of
new chromosomal DNA, but was an acquisition through lateral gene transfer.11 It produced a corrupted
message that gave bacteria a new ‘position’ in the gut. Y. pseudotuberculosis,
which lacks the hms locus gene inhabits harmlessly the midgut of the flea.
Plague bacilli, by contrast, have this inserted locus gene. Free from their original
control, causing a lack of ‘good’ ‘direction’ information,
the bacteria migrate from the midgut to the foregut, forming a plug of packed bacilli
which is passed on to the victim when the flea feeds.

Genes, germs and Genesis

Plague bacteria are not the only microorganisms that have degenerated into disease-causing
organisms. A more common recent example of a harmless bacteria ‘devolving’
into a pathogenic one is the intestinal Escherichia coli O157H7 strain
that occasionally causes fatalities.12
Other pathogenic bacteria that have undergone genomic decay include various mycoplasmas
(e.g. Mycoplasma genitalium and M. pneumonia, the later causing
pneumonia), and Mycobacterium leprae (the leprosy bacillus).13,14

As we study the origin of infectious disease from a creationist, biblical perspective,
bacteria provide us with a model of what may have happened to living things over
time in a fallen, cursed and corrupted world. Many illnesses can probably be traced
back to a loss of genetic information, plasmid acquisition, and gene translocation
in organisms such as bacteria, fungi, etc. For those who know the Creator, we can
rejoice that someday the Great Physician will restore all plagued bodies to a very
good condition once again(Rev. 22:2–3).

Recommended Resources

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People are told: ‘Evolution is happening all around us!’ This superb
presentation shows clearly that the examples used are actually the opposite of what
would support evolution. Both natural selection and mutation fit beautifully within
a biblical framework and are powerful tools to defend Genesis. (High School–Adult)
60 mins. While the content of this popular, illustrated presentation DVD is the
same as one you may have with the same title, it now includes extra features. Not
only does it have a new cover design, it also has English sub-titles, has been ‘re-badged’
to feature the CMI logo and contact details and includes a 3-minute promotional
segment.

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